Overexpression of PTEN suppresses non-small-cell lung carcinoma metastasis through inhibition of integrin αVβ6 signaling.

Studies have demonstrated that the abnormal expression of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is associated with multiple malignancies, but its functional role in non-small-cell lung carcinoma (NSCLC) metastasis remains to be elucidated. In the present study, we investigated the role of PTEN in regulating proliferation, migration, and invasion of NSCLC cells by establishing NSCLC cell strains with constitutively silenced or elevated PTEN expression. We demonstrated that ectopic expression of PTEN inhibits migration and invasion of NSCLC cells in vitro through wound healing and Transwell invasion assays. Furthermore, PTEN overexpression in NSCLC cells greatly inhibits cell viability and colony formation, which was confirmed by MTT and colony formation assays. Conversely, further analysis indicated that suppression of PTEN expression via shRNA promotes metastasis and growth of NSCLC cells. Finally, our findings demonstrate that PTEN promotes invasion and migration of NSCLC cells through the integrin αVβ6 signaling pathway. Overall, this study provides novel insights into the role of PTEN as a crucial regulator of NSCLC cell metastasis, and suggests that targeted treatment of PTEN-expressing tumors serves as a new therapeutic target for NSCLC.